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Fe deficiency is the most frequent nutritional d/o worldwide
Most of the Fe is absorbed in the duodenum, and Fe balance is largely maintained by regulation of absorptive intake
Forms of Fe in the body
Functional components
About 80% is in Hb
Mb and Fe-containing enzymes like catalase and cytochromes contain the rest
Storage components
Ferritin
Protein-Fe complex in liver, spleen, marrow, and skeletal muscle
In the liver, most of the ferritin is found in the parenchyma and comes from plasma transferrin
Elsewhere, ferritin is found in the macrophages and mostly comes from the breakdown of senescent or damaged RBCs
Serum [ferritin] is a good reflection of body Fe stores, but it is an acute phase reactant and it can become elevated with acute inflammation, even with Fe dietary deficiency
Hemosiderin
Located in lysosomes
This is what is mostly stained by special Fe stains (e.g., Prussian blue)
Causes of (-) Fe balance and anemia
Inadequate intake, poor absorption (e.g., sprue, gastrectomy), excessive demand (e.g., pregnancy), or chronic blood loss
Chronic blood loss is the most frequent cause in the US and this includes excessive menstrual losses and GI tract loss from ulcers and tumors
Effects of Fe deficiency are sequential
Depletion of storage Fe, followed by decreased serum [Fe] and decreased transferrin saturation (it’s normally 33% saturated), which will show up as a high total plasma Fe-binding capacity
Marrow sideroblasts disappear, leading to a microcytic, hypochromic anemia
Decreased Hb synthesis leads to elevation of free erythrocyte protoporphyrin (may help tell Fe deficiency from other causes of microcytosis, such as thalassemias and anemia of chronic disease
Depletion of Fe-containing enzymes may lead to koilonychias, alopecia, and atrophy of the tongue and GI tract mucosa, leading to malabsorption
Plummer-Vinson syndrome: Fe deficiency anemia, atrophic glossitis and esophageal webs
Category: Medical Subject Notes , Pathology Notes
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